ArticleCirculation research2010
CXCR4-mediated bone marrow progenitor cell maintenance and mobilization are modulated by c-kit activity.
Article in Circulation research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
36 citing papers in PubMed, 63 citations in OpenAlex.
- The role of SDF_1α/CXCR4 axis in non-antibody mediated TRALI in cardiac surgery patients.Intensive care medicine experimental · 2026Article
- Article
- Ablation of CXCR4 expression in cardiomyocytes exacerbates isoproterenol‑induced cell death and heart failure.International journal of molecular medicine · 2023Article
- Fluid Shear Stress Ameliorates Prehypertension-Associated Decline in Endothelium-Reparative Potential of Early Endothelial Progenitor Cells.Journal of cardiovascular translational research · 2022Article
- Temporal Gene Expression Profiles Reflect the Dynamics of Lymphoid Differentiation.International journal of molecular sciences · 2022Article
- Co-receptor signaling in the pathogenesis of neuroHIV.Retrovirology · 2021Review
- Ablation of lncRNATheranostics · 2021Article
- Visualization and Identification of Bioorthogonally Labeled Exosome Proteins Following Systemic Administration in Mice.Frontiers in cell and developmental biology · 2021Article
- Analysis of mesenchymal stem cell proteomesTheranostics · 2020Article
- Circulating myocardial microRNAs from infarcted hearts are carried in exosomes and mobilise bone marrow progenitor cells.Nature communications · 2019Article
- E2F1 Suppresses Oxidative Metabolism and Endothelial Differentiation of Bone Marrow Progenitor Cells.Circulation research · 2018Article
- Prostaglandin DNature communications · 2018Article
- CXCR-4 expression by circulating endothelial progenitor cells and SDF-1 serum levels are elevated in septic patients.Journal of inflammation (London, England) · 2018Article
- Mesenchymal Stem Cells Drive Cardiac Stem Cell Chemotaxis, Proliferation, and Phenotype via CXCR4 and cKit Signaling.Circulation research · 2016Article
- Dipeptidyl Peptidase-4 Inhibitor Increases Vascular Leakage in Retina through VE-cadherin Phosphorylation.Scientific reports · 2016Article
- SCF/c-kit transactivates CXCR4-serine 339 phosphorylation through G protein-coupled receptor kinase 6 and regulates cardiac stem cell migration.Scientific reports · 2016Article
- Exercise as an Adjuvant Therapy for Hematopoietic Stem Cell Mobilization.Stem cells international · 2016Review
- CXCR4 antagonist AMD3100 redistributes leukocytes from primary immune organs to secondary immune organs, lung, and blood in mice.European journal of immunology · 2015Article
- Directional migration of adult hematopoeitic progenitors to C6 gliomaOncology letters · 2015Article
- A critical role of Src family kinase in SDF-1/CXCR4-mediated bone-marrow progenitor cell recruitment to the ischemic heart.Journal of molecular and cellular cardiology · 2015Article
Corrections and comments
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Authors and funding
15 authors at 3 institutions in 2 countries.
Funding
Abstract
rationaleThe mobilization of bone marrow (BM) progenitor cells (PCs) is largely governed by interactions between stromal cell-derived factor (SDF)-1 and CXC chemokine receptor (CXCR)4. Ischemic injury disrupts the SDF-1-CXCR4 interaction and releases BM PCs into the peripheral circulation, where the mobilized cells are recruited to the injured tissue and contribute to vessel growth. BM PCs can also be mobilized by the pharmacological CXCR4 antagonist AMD3100, but the other components of the SDF-1-CXCR4 signaling pathway are largely unknown. c-kit, a membrane-bound tyrosine kinase and the receptor for stem cell factor, has also been shown to play a critical role in BM PC mobilization and ischemic tissue repair.
objectiveTo investigate the functional interaction between SDF-1-CXCR4 signaling and c-kit activity in BM PC mobilization. METHODS AND
resultsAMD3100 administration failed to mobilize BM PCs in mice defective in c-kit kinase activity or in mice transplanted with BM cells that expressed a constitutively active c-kit mutant. Furthermore, BM levels of phosphorylated (phospho)-c-kit declined after AMD3100 administration and after CXCR4 deletion. In cells adhering to culture plates coated with vascular cell adhesion molecule 1, SDF-1 and stem cell factor increased phospho-c-kit levels, and AMD3100 treatment suppressed SDF-1-induced, but not SCF-induced, c-kit phosphorylation. SDF-1-induced c-kit phosphorylation also required the activation of Src nonreceptor tyrosine kinase: pretreatment of cells with a selective Src inhibitor blocked both c-kit phosphorylation and the interaction between c-kit and phospho-Src.
conclusionsThese findings indicate that the regulation of BM PC trafficking by SDF-1 and CXCR4 is dependent on Src-mediated c-kit phosphorylation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.